Original Article: A study of right ventricular infarction in inferior wall myocardial infarction

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Original Article: A study of right ventricular infarction in inferior wall myocardial infarction Asif Iqbal, 1. Muddarangappa, 2 S.K.D. Shah, 2 Sudha Vidyasagar 1 1 Department of Medicine, Kasturba Medical College, Manipal, Karnataka, and 2 Department of Medicine, Sree Sidhartha Medical College, Tumkur, Karnataka INTODUCTION ight ventricular infarction (VI) was first recognized in a sub-group of patients with inferior wall myocardial infarction (MI) in whom right ventricle (V) failure and elevated right ventricular filling pressure despite of relatively normal left ventricular (LV) filling pressure was observed. Post-mortem studies revealed that there is V involvement in 19% to 51% of patients with acute inferior wall MI. VI contributes significantly to haemodynamic instability, atrioventricular (AV) block, bradycardia requiring pacing support and in-hospital mortality and morbidity. 1 The diagnosis of VI can be made from physical examination, echocardiography, first pass/ equilibrium radionuclide ventriculography, technetium pyrophosphate myocardial scintigram, haemodynamic measurements and angiography. But, right precordial electrocardio- ABSTACT Background: ight ventricular infarction (VI) is frequently associated with inferior wall myocardial infarction (MI). Methods: This study was designed to identify the burden of VI in patients presenting with inferior wall MI (n=50) by right precordial electrocardiogram (ECG) and comparing it with echocardiography (ECHO). esults: Their mean age was (54.5 ± 11.9 years); there were 42 males. ST elevation of greater than 1 mm in right precordial leads (PL) suggestive of VI was evident in 16 (32%) cases. Among the PL (V 3 - V 6 ) V 4 and V 5 showed sensitivity of 87.5%. The 12-lead ECG finding of ST-elevation greater than 1 mm in lead III and lead III/II greater than 1, had poor sensitivity (75%), specificity (88.2%) compared to ST- elevation of greater than 1 mm in any of the PL (100%). Both the echocardiography criteria, namely right ventricular end-diastolic dimension (VEDD) greater than 25 mm (92.3%) and the ratio of VEDD to left ventricular end-diastolic dimension (VEDD/LVEDD) greater than 0.7 (90%) indicating right ventricle (V) dilatation was observed significantly more frequently in VI group. Conclusions: VI occurs in more than one-third of patients with acute inferior wall MI. All the patients with inferior wall MI should have PL recorded as early as possible for evidence of VI, of which V4, V5 have the highest sensitivity. Key words: ight ventricular infarction, Electrocardiogram, ight precordial leads, Inferior wall myocardial infarction Iqbal A, Muddarangappa, Shah SKD, Vidyasagar S. A study of right ventricular infarction in inferior wall myocardial infarction. J Clin Sci es 2013;2:66-71. eceived: 30 October, 2012. 66 gram (ECG) is most readily available simple, routinely performed investigation and is of prognostic value. 1 It is important to recognize VI in patients presenting with inferior MI because, management of VI differs substantially from the management of LVMI. Keeping this in mind, the present study was designed to study the prevalence of VI among patients presenting with inferior wall MI using right precordial ECG and comparing it with echocardiography. MATEIAL AND METHODS Fifty patients presenting with inferior wall MI diagnosed on the basis of history, ECG, cardiac enzyme estimation and echocardiography 2,3 admitted to intensive care unit (ICU) of Sree Siddhartha Medical College and esearch Centre, Tumkur, during the period November 2007 to August 2009 were enrolled in the study. Institutional Ethics Committee approval was obtained to conduct the study. Corresponding Author: Dr Sudha Vidyasagar, Professor and Head, Department of Medicine, Kasturba Medical College, Manipal, Karnataka 574105 India. e-mail: vsagar33@yahoo.com

Patients with associated anterior and lateral wall MI, proved by ST elevation in anterior and lateral leads in ECG and wall motion abnormalities by echocardiography, a history of previous MI; ECG evidence of left bundle branch block (LBBB); cor-pulmonale; suspected pulmonary embolism; associated pericardial disease; and patients not consenting to participate were excluded from the study. VMI was diagnosed based on the criteria listed in Table 1. In all patients, a detailed history was taken and careful physical examination was done with special reference to haemodynamic parameters like jugular venous pulse (JVP), Kussmaul's sign, hypotension, presence of third and fourth heart sounds and cardiac murmur. They were also evaluated for coronary risk factors like smoking, hypertension, diabetes mellitus, obesity, alcohol and hypercholesterolaemia. In all of them 12-lead ECG, cardiac enzyme assay and echocardiography were carried out. The 12-lead ECG recordings were made at 25 mm/sec speed and 1 mv=10mm setting. ight precordial leads (PL) were applied on the right side of chest on the areas to which the leads corresponded on the left. Lead II ECG monitoring was done during the stay in ICU for identification of arrhythmias and conduction blocks. Echocardiography was done in all patients and compared with ECG findings. Coronary angiography was done in selected patients who could afford the procedure. Other laboratory investigations included random plasma glucose, fasting lipid profile, blood urea nitrogen, along with serum lactate dehydrogenase (LDH) and serum aspartate aminotransferase (AST), CKMB (immunoinhibition method; Erba creatine kinase-mb kit, Transasia biomedicals Ltd.); TOP I (lateral flow immunochromatic test, Instant view trop I whole blood/serum kit, Alfa scientific design). All patients with inferior wall MI were divided into VI and non VI group based on right precordial ECG findings. 67 Statistical analysis Table 1: Criteria for diagnosing VI ST segment elevation > 1mm in at least one of the right precordial leads V dilatation by 2D-echocardiography is given by VEDD > 25 mm and VEDD /LVEDD > 0.7 VI=right ventricular infarction VEDD=right ventricular end-diastolic dimension LVEDD=left ventricular end-diastolic dimension Source: references 2,3 Descriptive statistical analysis was carried out and results on continuous measurements have been presented on mean ± standard deviation (SD). esults on categorical measurements have been presented in number (%). Significance was assessed at 5 % level of significance. Chi-square, Fisher's exact tests were used to compare categorical variables. Sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV) and accuracy were computed for 12-lead ECG and PL, considering ST elevation greater than 1 mm in any of the PL as 'gold standard'. ESULTS Of the 50 cases with inferior wall MI, 16 (32%) cases had evidence of VI. Their mean age was 54.5 ± 11.9 years; there were 42 (84%) males. Most of the patients (30%) were in the age group of 51-60 years. Smoking was the major risk factor in 41 (82%) patients followed by hypertension in 22 (44%). They presented with chest pain (100%), sweating (86%) and syncope (2%) in VI group. Comparison of physical examination findings in patients with and without VI is shown in Table 2. ST elevation of greater then 1 mm in one of the PL indicating VI was evident in 16 cases, of which 6 cases showed ST elevation in all 4 leads, namely, V 3 - V 6 (Figure 1). ST-elevation was most commonly seen in lead V 4 and V 5 (87.5%) (Figure 2). In addition to PL, ST elevation of 1 mm or more in lead III, ratio III/II greater than 1 was found in the 12-lead ECG in 14 patients (58.3%) in VI group and 10 patients (41.7%) in non-vi group. Echocardiography criteria 3 of VI, suggestive

Table 2: Comparison of physical examination findings at presentation in patients with and without VI With Without Physical findings VI VI p-value (n=16) (n=32) Pulse (/min) <60 3 2 0.377 60-90 11 26 >90 2 6 Systolic blood pressure (mm Hg) Low (<90) 3 2 0.398 Normal (91-140) 12 30 High (>140) 1 2 Tachypnoea 4 9 1.000 Jugular Venous Pulse Elevated 4 3 0.190 Kussumaul's sign positive 5 0 0.002 Basal crepitations 1 3 1.000 VI= right ventricular infarction of V dilatation was observed in both the groups. Thirteen patients showed right ventricular end-diastolic dimension, (VEDD) greater than 25 mm indicating V dilation of which 10 (92.3%) had evidence of V infarction. Also, 9 of the 10 patients with ratio of VEDD to left ventricular end-diastolic dimension, (VEDD/LVEDD) greater than 0.7 had evidence of VI. Table 3 shows the sensitivity, specificity, PPV, NPV and accuracy of 12-lead ECG criteria and PL in diagnosing VI. Comparison of the sensitivity of right precordial leads (V 3 - V 6 ) in diagnosing VI in the present study and other published studies is shown in Table 4. 68 Complications like sinus bradycardia, atrioventricular block, asystole and multiple ventricular premature complexes (VPCs) in patients 1, 4-9 with and without VI is shown in Table 5. DISCUSSION In the present study, VI was evident in 32% of cases with inferior wall MI. A similar prevalence of VI of 30% 10 and 37% 11 has been reported in other studies in patients with inferior wall MI. VI is less common since V is less susceptible to ischaemia as oxygen demand is significantly lesser because of its smaller muscle mass 12,13 and coronary perfusion in right ventricle occurs in both systole and diastole. 14 Most of the cases (46.7%) of VI occurred in the age group of 51-60 years in the VI group compared to non-vi that was commonly (84.6%) seen in the age group of 41-50 years. In the present study 84% were males. Similar Table 3: Diagnostic yield of 12-lead ECG and right precordial leads in diagnosing VI ECG Criteria Sensitivity Specificity PPV NPV Accuracy p-value ST 1mm in lead III, in 75.0 88.2 75.0 88.2 84.0 <0.001 lead III/II>1 V3 37.5 100 100 77.3 80.0 <0.001 V4 87.5 100 100 94.4 96.0 <0.001 V5 87.5 100 100 94.4 98.0 <0.001 V6 75.0 100 100 89.5 92.0 <0.001 * ST elevation > 1 mm in any of the right precordial leads was considered as gold standard ECG= electrocardiogram; VI= right ventricular infarction; PPV= positive predictive value; NPV= negative predictive value

Figure 2: Evidence of ST elevation > 1 mm in individual PL in patients with right ventricular infarction PL=right precordial leads Figure 1: Electrocardiogram in a patient with inferior wall MI with right ventricular involvement showing (A) ST-elevation in leads II, III, avf, lead III/II >1 (B) ST-elevation in right precordial leads (V 3 - V 6 ) indicating right ventricular involvement 69 male preponderance (86%) was reported in another study. 15 Among the 42 male patients in our study 13 (31 %) had VI while only 3 of the 8 women (37.5%) had evidence of VI; however, this difference did not attain statistical significance. In another study, 16 it was observed that prevalence of VI increased as age advanced and prognostic effect of VI was independent of gender. All the patients in the study presented with chest pain. Prevalence of VI was associated more with vomiting (41.6%), breathlessness (40%) and syncope (100%). A patient with VI who also had complete heart block presented with syncope. Patients with VI and complete heart block have been observed to present with episodes of syncope classically described as Stokes-Adams attack. 17 In the present study among PL, V 3 had sensitivity of 37% and lead V 4 and V 5 showed sensitivity of 87.5% for identifying ST elevation greater than 1 mm suggestive of VI (Table 3). In most studies (Table 4) 1,4-9 lead V 4 was found to be the most sensitive among all PL in detecting VI (Table 4). An ST segment which is higher in lead V 4 than in leads V I to V 3 offers the highest specificity and efficiency in diagnosis. 2 Comparing the reliability of 12-lead ECG criteria with that of PL in diagnosing VI, we found that 12-lead ECG finding of ST elevation greater than 1 mm in lead III, ST elevation in lead III/II greater than 1, had poor sensitivity (75%), specificity (88.2%), PPV(75%), NPV (88.2%) and accuracy (84%). In a study 19 evaluating the reliability of 12-lead ECG criteria in the diagnosis of VI, it was found that the right sided chest leads had a higher specificity and PPV than inferior leads, but poor sensitivity, NPV, and accuracy. However, the differences were not statistically significant. In right chest leads recognition of infarction signals is easy because only the presence of ST elevation of 1 mm or more is re-

quired to diagnose VI but in inferior leads a difference between ST elevation in two leads must be interpreted. Thus right precordial leads appear to be a better indicator of VI than 12- lead ECG. In the present study, among patients in whom VI was confirmed by echocardiography criteria, 3 PL evidence of VI was evident in more than 90 percent of cases. In another study 20 of 42 inferior wall MI patients, 16 had an echocardiography evidence suggestive of V dilatation; this included 12 with V 4 evidence of VI. Cardiogenic shock was the cause of death in 2 cases in our study of which 1 had evidence of V involvement. It has been observed that inferior wall MI patients who also have V myocardial involvement are at risk of death, cardiogenic shock and arrhythmia. 21 Among the 8 patients with inferior wall MI treated with volume replacement, 6 had evidence of VI in the present study. Patients with VI who are haemodynamically unstable should be managed with volume loading to maintain adequate V preload as preload determines V output. Any interventions that reduce the preload, like diuretics, nitrates and vasodilators should be avoided even in the absence of hypotension as this will lead to worsening of symptoms. This treatment strategy would differ from therapy for pump failure caused by acute left ventricular infarction due to need for maintaining the V preload in acute V infarction. 22 Our observations suggest that VI occurs in more than one-third of patients with acute inferior wall MI. A spectrum of disease from asymptomatic mild right ventricular dysfunction to cardiogenic shock has been recognized. All the patients with inferior wall MI should have right sided precordial leads recorded as early as possible for evidence of VI, of which V 4 and V 5 have highest sensitivity. The diagnosis can be further confirmed by echocardiography for V dilatation thus helping in preventing the complications and mortality associated with it. Table 4: Comparison of sensitivity of leads V 3 and V 4 in the diagnosis of VI Study Year Sensitivity in leads% V 3 V 4 V 5 Braat et al 4 1983 69 93 Klein et al 5 1983 83 Anderson et al 6 1983 37 33 Morgen et al 7 1984 100 Braat et al 8 1984 80 72 Gupta et al 9 1990 88.8 100 Zehender et al 1 1993 88 72 Present study 37 87.5 87.5 VI=right ventricular infarction Table 5: Comparison of complications in patients with and without VI Complications With Without p-value VI VI (n=16) (n=34) Multiple VPC 1 1 NS 1 o heart block 2 6 NS 2 o heart block 1 0 0.320 Complete heart block 1 1 0.542 Asystole 2 0 0.098 Sinus tachycardia 0 1 1.000 Sinus bradycardia 3 2 0.311 VPC=ventricular premature contractions; VI=right ventricular infarction; VF=ventricular fibrillation 70

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